SUMMARY
During infection, Staphylococcus aureus forms dense multicellular structures, called staphylococcal abscess communities (SACs), that are encased in a capsule made of host fibrin to evade host immune defenses. S. aureus cells divide characteristically along successive orthogonal planes, but the contribution of this division geometry to infection is unclear. Here, we show that disrupting orthogonal cell division by deleting the cell division septum placement factor PcdA impairs SAC formation in vivo and in a three-dimensional in vitro model. Loss of PcdA leads to uneven surface distribution of adhesins containing the YSIRK signal sequence that directs their insertion into the division septum, thereby resulting in uneven interaction with fibrin fibers. Consequently, bacterial communities fail to establish a robust fibrin pseudocapsule and remain accessible to immune cells. We propose that orthogonal cell division coordinates cell cycle progression with extracellular matrix engagement, SAC architecture, and persistence within host tissues.
HIGHLIGHTS
Orthogonal cell division promotes staphylococcal abscess community formation
Loss of PcdA disrupts fibrin pseudocapsule assembly in 3D models
Division geometry ensures uniform surface deployment of adhesins
Cell division plane selection links bacterial cell cycle control to virulence
Full Text
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